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Biomedical subjects

H Luo

Publications and source records attributed to H Luo.

At least 163 records · Page 9Linked to original sources
PubMed1996

Antibodies against retroviral proteins and nuclear antigens in a subset of idiopathic CD4+ T lymphocytopenia patients.

Idiopathic CD4+ T lymphocytopenia (ICL) is an immunodeficiency syndrome characterized by severe depletion of CD4+ T lymphocytes, but in which human immunodeficiency virus cannot be detected. Peripheral blood mononuclear cells (BPMCs) from an ICL patient were cocultured with HUT78 T-lymphoblastoid cells, and an acute cytopathic effect and formation of multinucleated cells were observed. A human intracisternal A-type retroviral particle designated HIAP-II was detected in cells surviving the acute cytopathic effect. Eight of 13 ICL patients in a blinded screen of a serological panel provided by the National Centers for Disease Control and Prevention (CDC) had serum antibodies that specifically reacted with HIAP-II associated proteins by Western immunoblotting. None of 19 control sera in the panel that were unreactive with HIV Gag proteins produced a positive result on HIAP-II immunoblots. Comparable results were obtained in a blinded screen of a second CDC serological panel. Sera from 8 of 14 ICL patients in the second serological panel were positive for antinuclear autoantibodies (ANAs) commonly observed in patients with systemic autoimmune diseases. These results suggest the possible involvement of an A-type retrovirus or autoimmunity in development of ICL in a subset of patients.

Adult↗
PubMed1996

A JAK-STAT pathway regulates wing vein formation in Drosophila.

We present evidence that the JAK-STAT signal transduction pathway regulates multiple developmental processes in Drosophila. We screened for second-site mutations that suppress the phenotype of the hyperactive hopTum-1 Jak kinase, and recovered a mutation that meiotically maps to the known chromosomal position of D-Stat, a Drosophila stat gene. This hypomorphic mutation, termed statHJ contains a nucleotide substitution in the first D-Stat intron, resulting in a reduction in the number of correctly processed transcripts. Further, the abnormally processed mRNA encodes a truncated protein that has a dominant negative effect on transcriptional activation by the wild-type cDNA in cell culture. statHJ mutants exhibit patterning defects that include the formation of ectopic wing veins, similar to those seen in mutants of the epidermal growth factor/receptor pathway. Abnormalities in embryonic and adult segmentation and in tracheal development were also observed. The hopTum-1 and statHJ mutations can partially compensate for each other genetically, and Hop overexpression can increase D-Stat transcriptional activity in vitro, indicating that the gene products interact in a common regulatory pathway.

Animals↗
PubMed1996

Expression of human mitochondrial NADP-dependent isocitrate dehydrogenase during lymphocyte activation.

In the process of identifying genes involved in optimization of lymphocyte activation, we have cloned the human mitochondrial NADP-dependent isocitrate dehydrogenase (mNADP-IDH) cDNA. The cDNA and its deduced amino acid (AA) sequence had a high degree of homology with those of the porcine and bovine. The heart and muscle had the highest constitutive expression of the gene. The expression of steady-state mRNA in the resting T and B lymphocytes was low but was induced after mitogen stimulation. The mRNA levels peaked around 48 h and remained elevated at 72 h. At the protein level, the mitochondrial but not cytosolic NADP-IDH activity was augmented after the mitogen stimulation. There was no cell cycle-dependent fluctuation of mNADP-IDH expression in synchronized Jurkat cells. In T and B cells, rapamycin (RAPA) could repress the mitogen-stimulated mNADP-IDH expression, although most of the early or late phase activation-related genes including a G-protein beta subunit-related gene H12.3 were not affected by the drug. The restricted expression of the gene in certain tissues and the activation-related expression in lymphocytes suggest that this gene might be necessary for optimal functions in heart, muscle, and the activated lymphocytes.

Amino Acid Sequence↗
PubMed1996

Molecular cloning of the cDNA of mouse mitochondrial NADP-dependent isocitrate dehydrogenase and the expression of the gene during lymphocyte activation.

The current report documents the molecular cloning of the mouse mitochondrial NADP-dependent isocitrate dehydrogenase (mNADP-IDH) cDNA. The cDNA was 1,863 bp in length and contained one open reading frame encoding a 523-residue polypeptide with a predicted molecular weight of 58 kDa. The cDNA and the deduced amino acid (AA) sequence of the mouse mNADP-IDH had a high degree of homology with those of porcine, bovine, alfalfa, and yeast. The recombinant mNADP-IDH expressed in Escherichia coli had active enzymatic function, as well as an expected molecular weight. The heart had the highest constitutive expression of the steady-state mNADP-IDH mRNA, followed by the kidney, while the expression of the gene in other tissues was low. The enzymatic activity of different tissues was in agreement with their mNADP-IDH mRNA levels. The resting lymphocytes had low constitutive expression of the gene, but the steady-state mRNA could be induced 48 h after mitogen stimulation. At the protein level, the resting lymphocytes had low enzymatic activity of mNADP-IDH, but the activity was augmented fivefold after mitogen stimulation. The cytosolic NADP-IDH, on the contrary, remained low or undetectable before and after the mitogen stimulation. Based on our current findings as well as the known roles of the mNADP-IDH in anabolism and in the isocitrate shuttle, it is conceivable that the mNADP-IDH is necessary for optimizing proliferation in lymphocytes.

Amino Acid Sequence↗
PubMed1996

Absence of focal compensatory enlargement or constriction in diseased human coronary saphenous vein bypass grafts. An intravascular ultrasound study.

BACKGROUND: No in vivo data are available on the occurrence of compensatory enlargement or vessel constriction in diseased human coronary saphenous vein bypass grafts (SVBGs). The aim of this intravascular ultrasound (IVUS) study was to examine to what extent lumen reduction is accompanied by (1) vessel wall thickening and (2) arterial wall constriction in SVBGs. METHODS AND RESULTS: We used IVUS to examine 43 SVBGs from 42 patients (32 men, 10 women; mean age, 72 +/- 5 years) 8 to 23 (11 +/- 4) years after SVBG. IVUS images were obtained with a 3.5F monorail ultrasound catheter with a 30-MHz frequency and were analyzed at the lesion site, the reference site, and an intermediate site. The lumen area was significantly (P < .01) decreased; the vessel wall area (SVBG cross-sectional area minus lumen area) and the plaque area (area within the external elastic lamina minus lumen area) were significantly (P < .01) increased from the reference site through the lesion site. However, SVBG cross-sectional area was the same at these three sites (24.0 +/- 8.1 versus 24.4 +/- 8.6 versus 24.5 +/- 8.6 mm2, P = NS), and the external elastic lamina area was also quite constant in each vessel (17.8 +/- 6.0 versus 17.7 +/- 6.4 versus 17.6 +/- 6.2 mm2, P = NS). CONCLUSIONS: These in vivo IVUS data from human coronary SVBGs demonstrate that (1) no focal compensatory enlargement or vessel constriction occurred in stenotic segments compared with the reference segments and that (2) the absence of focal compensatory enlargement appears to be a potentially important factor in the progression of stenoses in coronary SVBGs.

Aged↗
PubMed1996

Effect of External Ultrasound Frequency on Thrombus Disruption In Vitro.

Objectives: This in vitro study assesses the effect of different external ultrasound frequencies on the disruption of human thrombi. Background: Ultrasound energy has been shown to disrupt human thrombi in vitro. However, there have been no previous studies to assess the effect of a range of different ultrasound frequencies on the rate and extent of thrombus disruption. Methods: In vitro, we exposed 56, 1- to 3-hour-old human blood thrombi to continuous wave ultrasound (2.9 W/cm2) for 3 minutes. Seven different frequencies, ranging from 243 kHz to 25 kHz, were used. Results: There was a gradual increase in the total reduction of thrombus weight as well as the percent thrombus disruption with the use of lower ultrasound frequencies, reaching 99% at 25 kHz (p < 0.001) and 86% (p < 0.001) at 39 kHz, compared with 25% at 243 kHz. The average particle size of the disrupted thrombi was 3.26 µm (range 2.8-3.8). Conclusions: Our in vitro data with external ultrasound show that for a given power intensity of ultrasound, the extent and magnitude of thrombus disruption is progressively increased as frequencies decrease from 243 to 25 kHz. This might be related to the fact that larger acoustic bubbles are induced by lower frequency ultrasound, which gives rise to greater mechanical energy for thrombus disruption during bubble vibration and their collapse.

Journal Article↗
PubMed1996

Role of chromium(IV) in the chromium(VI)-related free radical formation, dG hydroxylation, and DNA damage.

A reactive Cr(IV) ester was synthesized from a reaction of CrO3 with 2,4-dimethyl-2,4-pentanediol as verified by electron spin resonance (ESR) and magnetic susceptibility measurements. ESR spin trapping studies demonstrate that the Cr(IV) ester is capable of generating hydroxyl free radical (.OH) through a Fenton-like mechanism (Cr(IV)+H2O2-->Cr(V)+.OH+OH-) with a concomitant generation of Cr(V) species (g = 1.9787). Cr(IV) caused DNA strand breaks as measured by electrophoretic assays. H2O2 enhanced the DNA strand breaks via .OH formation by a Cr(IV)-mediated Fenton-like reaction. In the Cr(IV)/H2O2 system, formate did not block Cr(V) formation, but prevented DNA damage, indicating that .OH radicals, and not Cr(V), caused the DNA damage. Reaction of Cr(VI) with ascorbate was also used as a source of Cr(IV). Incubation of Cr(VI), ascorbate, and DNA caused DNA strand breaks. A free radical trap, 5,5-dimethyl-1-pyrroline (DMPO), only slightly inhibited the DNA damage. Addition of Mn(II), which inhibited Cr(IV), caused significant protection. H2O2 enhanced the DNA damage via Cr(IV)-mediated .OH radical generation and Mn(II) inhibited the damage, again showing that Cr(IV) and its related .OH generation caused DNA strand breaks. HPLC measurements showed that .OH radicals generated by a Cr(IV)-mediated Fenton-like reaction generated 8-hydroxy-2'-deoxyguanosine from 2'-deoxyguanosine. The results demonstrate that Cr(IV) and its generated .OH radicals are capable of damaging DNA. Moreover, in comparison with Cr(V), Cr(IV) is a more potent DNA damaging agent.

Chromium↗
PubMed1996

Contribution of inadequate compensatory enlargement to development of human coronary artery stenosis: an in vivo intravascular ultrasound study.

OBJECTIVES: This intravascular ultrasound study sought to examine to what extent native coronary artery stenosis is accompanied by vessel wall thickening or inadequate compensatory enlargement (relative vessel constriction), or both. BACKGROUND: In human femoral arteries, inadequate compensatory enlargement is reported to be a paradoxic mechanism for the development of severe arterial lumen narrowing. However, it is unclear in human coronary arteries whether inadequate compensatory enlargement contributes to the development of critical arterial stenosis. METHODS: Thirty-five primary coronary artery lesions from 30 patients (19 men, 11 women; mean [+/- SD] age 65 +/- 13 years) were imaged by intravascular ultrasound. The vessel cross-sectional area and lumen area were measured, and the wall area (vessel cross-sectional area minus lumen area) was calculated at the lesion site and at the proximal and distal reference sites. We defined compensatory enlargement to be present when the vessel cross-sectional area at the lesion site was larger than that at the proximal reference site, inadequate compensatory enlargement when the vessel cross-sectional area at the lesion site was smaller than that at the distal reference site and intermediate remodeling when the vessel cross-sectional area at the lesion site was intermediate between the two reference sites. RESULTS: Compensatory enlargement was observed in 19 (54%) of 35 lesions, inadequate compensatory enlargement in 9 (26%) of 35 and intermediate remodeling in 7 (20%) of 35. In the inadequate compensatory enlargement group, reduction of the vessel cross-sectional area contributed to 39% of lumen reduction. CONCLUSIONS: Compensatory enlargement commonly (54%) occurs at stenotic coronary lesions. However inadequate compensatory enlargement results in a substantial amount (39%) of the lumen area reduction in 26% of primary coronary artery lesions.

Adult↗
PubMed1996

Evaluation of 1-azabicyclo[2.2.2]oct-3-yl alpha-fluoroalkyl-alpha-hydroxy-alpha-phenylacetates as potential ligands for the study of muscarinic receptor density by positron emission tomography.

Both 1-azabicyclo[2.2.2]oct-3-yl alpha-(1-fluoroeth-2-yl)-alpha-hydroxy-alpha-phenylacetate (FQNE, 5) and 1-azabicyclo[2.2.2]oct-3-yl alpha-(1-fluoropent-5-yl)-alpha-hydroxy-alpha-phenylacetate (FQNPe, 6) were prepared and evaluated as potential candidates for the determination of muscarinic cholinergic receptor (mAChR) density by positron emission tomography (PET). The results of in vitro binding assays demonstrated that although both 5 and 6 had high binding affinities for m1 and m2 mAChR subtypes, 6 displayed a higher affinity (nM, m1; KD, 0.45, m2; KD, 3.53) as compared to 5 (nM, m1; KD, 12.5, m2; KD, 62.8). It was observed that pretreatment of female Fisher rats with either 5 or 6 prior to the i.v. administration of Z-(-)(-)-[131I]-IQNP, a high-affinity muscarinic ligand, significantly blocked the uptake of radioactivity in the brain and heart measured 3 h postinjection of the radiolabeled ligand. These new fluoro QNB analogues represent important target ligands for evaluation as potential receptor imaging agents in conjunction with PET.

Animals↗
PubMed1996

Correspondence of aortic valve area determination from transesophageal echocardiography, transthoracic echocardiography, and cardiac catheterization.

The correspondence of aortic valve area measurements from transesophageal echocardiography, transthoracic echocardiography, and cardiac catheterization was determined in 100 patients with severe aortic stenosis (aortic valve area < or = 0.75 cm2), moderate aortic stenosis (aortic valve area > 0.75 to < or = 1.2 cm2), mild aortic stenosis (aortic valve area > 1.2 to < or = 2.0 cm2), and nonstenotic aortic valves (aortic valve area > 2.0 cm2). Because high correlation does not require high agreement, data were assessed by analysis of agreement. Aortic valve areas determined by transthoracic echocardiography (1.43 +/- 0.76 cm2), transesophageal echocardiography (1.40 +/- 0.79 cm2), and cardiac catheterization (1.47 +/- 0.82 cm2) were similar. Correlations between methods were excellent (r values = 0.96). "Limits of agreement" between the three comparisons did not differ significantly. Similar levels of agreement when comparing these independent methods for determining the aortic valve area indicate that direct planimetry by transesophageal echocardiography, the continuity equation with transthoracic echocardiography, and the Gorlin formula are equally accurate and may be used interchangeably. Clinically important discrepancies between methods are uncommon and are readily settled by adding a third method.

Adult↗
PubMed1996

Heat shock pretreatment prevents hydrogen peroxide injury of pulmonary endothelial cells and macrophages in culture.

The purpose of the present study was to determine whether heat shock pretreatment would protect pulmonary endothelial cells and alveolar macrophages against hydrogen peroxide (H2O2)-induced injury. The bovine pulmonary artery endothelial cells (BPAECs) heat-shocked (42 degrees C for 2 h) prior to exposure to H2O2 (1 mmol/L for 45 min) showed significant decrease in H2O2-mediated increment of release of lactate dehydrogenase and production of thiobarbituric acid-reactive substances, and obvious alleviation in H2O2-induced decrease in activities of catalase and superoxide dismutase. Heat-shocked (42 degrees C for 2 h) rat pulmonary alveolar macrophages (PAMs) also obtained acquired resistance to injury by subsequent exposure of 1, 2, or 3 mmol/L H2O2 for 45 min. Simultaneously with this acquired oxidative resistance, Northern blot analysis showed that heat-shocked BPAECs and PAMs, contained an increased level of mRNA coding for the inducible form of heat shock protein 70 (HSP70), and Western blot analysis indicated that there were increased expression of HSP70. Inhibition of protein synthesis by cycloheximide (25 micrograms/mL) and inhibition of RNA synthesis by actinomycin D (5 micrograms/mL) prevented the cytoprotection against H2O2. These results are consistent with the hypothesis that heat shock pretreatment would protect pulmonary endothelial cells and alveolar macrophages against H2O2-induced injury, and possibly that HSPs play a role in this cytoprotection.

Animals↗
PubMed1996

Coronary artery restenosis after balloon angioplasty in humans is associated with circumferential coronary constriction.

Therapies that inhibit intimal hyperplasia do not prevent restenosis after coronary artery balloon angioplasty, suggesting that additional mechanisms may be responsible for restenosis in humans. Using an intravascular ultrasound (Hewlett-Packard Sonos Intravascular Imaging System). 3.5F, 30-MHz (Boston Scientific) monorail imaging catheter, we studied 17 patients with clinical and angiographic restenosis at an average (mean +/- SD) of 7 +/- 6 months after balloon angioplasty (13 men age, 71 +/- 10 years; 12 left anterior descending coronary arteries, 4 right coronary arteries, and 1 left circumflex coronary artery) The lumen area (L.A), vessel wall area (VWA), and total cross-sectional area (CSA) within the external elastic lamina were measured at the restenosis site and at proximal and distal reference sites, which were defined as adjacent segments with the least amount of plaque. Consistent with coronary angiography findings, decreased LA at the restenotic site was detected in all 17 patients. The unique finding was that total CSA at the restenotic site was significantly decreased compared with both proximal and distal reference sites (10.1 +/- 2.4 versus 14.8 +/- 3.2 mm2 and 10.1 +/- 2.4 versus 13.8 +/- 3.1 mm2, respectively, P < .001), whereas VWA (intima plus media) was slightly increased at the angioplasty site compared with both proximal and distal reference sites (8.0 +/- 2.3 versus 7.6 +/- 2.3 mm2 and 8.0 +/- 2.3 versus 6.7 +/- 2.3 mm2, respectively, P = NS). Eighty-three percent of the loss in LA at the restenotic site was due to constriction of the total CSA, while the increase in VWA at the restenotic site accounted for only a 17% loss in LA. We then compared these results with the morphology of coronary artery segments in 14 patients without restenosis. These coronary artery segments had been previously treated with balloon angioplasty (7 +/- 5 months). Unlike that in restenotic lesions, the total CSA within the external elastic lamina at the sites of previous angioplasty was similar to that in distal and proximal reference sites (P = NS). Significant and consistent reduction in arterial CSA, with a minor increase in VWA, characterizes human coronary lesions that cause angiographic restenosis. These data suggest that in humans, "recoil" and/or vascular contraction with healing in response to balloon injury is a major contributor to restenosis after balloon angioplasty.

Aged↗
PubMed1996

[Analysis of the A/C polymorphic site within the phenylalanine hydroxylase gene].

An A/C polymorphism was identified at nucleotide-11 from the acceptor site of IVS3 of the phenylalanine hydroxylase gene. This polymorphism can be detected easily by means of single strand conformation polymorphism analysis. The frequency for the majior allele (A) was 0.656 and 0.344 for the minor allele (C) with the PIC being 0.351 in Chinese population. There was no linkage disequilibrium between this site and the STR polymorphic site located upstream within the same intron of the gene. The ejjicincy of prenatal gene diagnosis fro PKU was estimated to be 78.1% by haplotype linkage analysis using these two polymorphic sits.

Humans↗
PubMed1996

Repeated recurrence of osteosarcoma treated by resections and chemotherapy.

This paper presents 5 patients with repeated recurrence of osteosarcoma (RROS). The primary focus of 3 patients were in the distal portion of femur, and 2 patients were in the proximal portion of tibia. Three patients, whose chest X ray film were negative, were treated by amputation and chemotherapy. Two patients had isolated metastatic focus 1.5 cm in diameter in lung, were treated by amputation after 1 week of chemotherapy and then treated by lobectomy after 2 weeks of chemotherapy. After operation, the chemotherapy was carried out for 3 courses of treatment. The roentgenogram of chest and affected limb were taken once every two months. There were metastatic focuses found in the lung of 1 patient and in the distal portion of femur of 2 patients. One patient was operated on for 4 times. Up to now, 3 patients have been living for 5 years and 2 patients for 6 years after operation.

Adolescent↗